A Phase 3, Randomized, Double-blind, Placebo-controlled, Multicenter Study to Evaluate the Efficacy and Safety of Amyloid Depleter ALXN2220 in Adult Participants with Transthyretin Amyloid Cardiomyopathy (ATTR-CM) - ALXN2220-ATTRCM-301

开始日期2024-05-14

申办/合作机构

Alexion Pharmaceuticals, Inc.

NCT06183931 / Recruiting临床3期

A Phase 3, Randomized, Double-blind, Placebo-controlled, Multicenter Study to Evaluate the Efficacy and Safety of Amyloid Depleter ALXN2220 in Adult Participants With Transthyretin Amyloid Cardiomyopathy (ATTR-CM)

The primary objective of this study is to access the efficacy of ALXN2220 in the treatment of adult participants with ATTR-CM by evaluating the difference between the ALXN2220 and placebo groups as assessed by the total occurrences of ACM and CV clinical events.

开始日期2024-01-11

申办/合作机构

Alexion Pharmaceuticals, Inc.

100 项与 NI-006 相关的临床结果

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100 项与 NI-006 相关的转化医学

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100 项与 NI-006 相关的专利（医药）

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项与 NI-006 相关的文献（医药）

2024-09-01·Current Opinion in Cardiology

Treatment of transthyretin cardiac amyloidosis

Review

作者: Maurer, Mathew S ; Wardhere, Abdirahman ; Bampatsias, Dimitrios

Purpose of reviewTafamidis is currently the only approved disease-modifying treatment for ATTR-CM. However, there have been important developments in the treatment of ATTR-CM, as the results of two phase 3 trials were published and several other trials are in their final stages. In this review, we summarize current and future therapies for ATTR-CM.Recent findingsRecently, acoramidis, a TTR stabilizer has been proven to be effective in reducing mortality and morbidity compared to placebo in the ATTRibute-CM trial. Additionally, patisiran, an RNA silencer, preserved functional capacity and quality of life compared to placebo in the APOLLO-B trial. However, the FDA declined to approve patisiran for ATTR-CM. The results of phase 1 trial of ALXN2220, an antiamyloid antibody raise hope for reversal of myocardial damage by amyloid depletion. Phase 3 trials evaluating the efficacy of different RNA silencers, gene editing with CRISPR-Cas9, and other anti-amyloid antibodies are ongoing.SummaryTherapies targeting different mechanism in the pathophysiology of ATTR-CM provide new alternatives for treating patients with ATTR-CM. Future research should focus on comparing their effectiveness, the potential of combined treatment with agents from different classes and on identifying the patients who will benefit most from each class of medication.

2023-07-20·New England Journal of Medicine1区 · 医学

Phase 1 Trial of Antibody NI006 for Depletion of Cardiac Transthyretin Amyloid

1区 · 医学

Article

作者: Mercuri, Michele F ; Lairez, Olivier ; Kristen, Arnt V ; Donal, Erwan ; Aus dem Siepen, Fabian ; van der Meer, Peter ; Garcia-Pavia, Pablo ; Hock, Christoph ; Grimm, Jan ; Michalon, Aubin ; Frost, Robert J A ; Nitsch, Roger M ; Kahr, Peter C ; Damy, Thibaud

BACKGROUNDTransthyretin amyloid (ATTR) cardiomyopathy is a progressive and fatal disease caused by misfolded transthyretin. Despite advances in slowing disease progression, there is no available treatment that depletes ATTR from the heart for the amelioration of cardiac dysfunction. NI006 is a recombinant human anti-ATTR antibody that was developed for the removal of ATTR by phagocytic immune cells.METHODSIn this phase 1, double-blind trial, we randomly assigned (in a 2:1 ratio) 40 patients with wild-type or variant ATTR cardiomyopathy and chronic heart failure to receive intravenous infusions of either NI006 or placebo every 4 weeks for 4 months. Patients were sequentially enrolled in six cohorts that received ascending doses (ranging from 0.3 to 60 mg per kilogram of body weight). After four infusions, patients were enrolled in an open-label extension phase in which they received eight infusions of NI006 with stepwise increases in the dose. The safety and pharmacokinetic profiles of NI006 were assessed, and cardiac imaging studies were performed.RESULTSThe use of NI006 was associated with no apparent drug-related serious adverse events. The pharmacokinetic profile of NI006 was consistent with that of an IgG antibody, and no antidrug antibodies were detected. At doses of at least 10 mg per kilogram, cardiac tracer uptake on scintigraphy and extracellular volume on cardiac magnetic resonance imaging, both of which are imaging-based surrogate markers of cardiac amyloid load, appeared to be reduced over a period of 12 months. The median N-terminal pro-B-type natriuretic peptide and troponin T levels also seemed to be reduced.CONCLUSIONSIn this phase 1 trial of the recombinant human antibody NI006 for the treatment of patients with ATTR cardiomyopathy and heart failure, the use of NI006 was associated with no apparent drug-related serious adverse events. (Funded by Neurimmune; NI006-101 ClinicalTrials.gov number, NCT04360434.).

World Journal of Cardiology

Recent advances in the diagnostic methods and therapeutic strategies of transthyretin cardiac amyloidosis

作者: Skoularigis, John ; Xanthopoulos, Andrew ; Magouliotis, Dimitrios E ; Kourek, Christos ; Giamouzis, Grigorios ; Georgoulias, Panagiotis ; Briasoulis, Alexandros ; Triposkiadis, Filippos

Cardiac amyloidosis is a progressive disease characterized by the buildup of amyloid fibrils in the extracellular space of the heart. It is divided in 2 main types, immunoglobulin light chain amyloidosis and transthyretin amyloidosis (ATTR), and ATTR amyloidosis is further divided in 2 subtypes, non-hereditary wild type ATTR and hereditary mutant variant amyloidosis. Incidence and prevalence of ATTR cardiac amyloidosis is increasing over the last years due to the improvements in diagnostic methods. Survival rates are improving due to the development of novel therapeutic strategies. Tafamidis is the only disease-modifying approved therapy in ATTR amyloidosis so far. However, the most recent advances in medical therapies have added more options with the potential to become part of the therapeutic armamentarium of the disease. Agents including acoramidis, eplontersen, vutrisiran, patisiran and anti-monoclonal antibody NI006 are being investigated on cardiac function in large, multicenter controlled trials which are expected to be completed within the next 2-3 years, providing promising results in patients with ATTR cardiac amyloidosis. However, further and ongoing research is required in order to improve diagnostic methods that could provide an early diagnosis, as well as survival and quality of life of these patients.

项与 NI-006 相关的新闻（医药）

2024-11-14

·生物探索

Nature Biotechnology | 淀粉样蛋白沉积为何如此难治，研究人员找到了哪些突破？

引言淀粉样蛋白（amyloid）一直是一个备受关注的研究课题，其异常堆积与多种严重疾病密切相关。近年来，研究人员在治疗淀粉样蛋白相关疾病方面取得了显著进展，尤其在心力衰竭、肌萎缩侧索硬化症（ALS）以及阿尔茨海默病（Alzheimer's disease）等领域的突破性研究令人振奋。11月11日 Nature Biotechnology “Amyloid is everywhere, but new treatments could stop the toxic build up”深入探讨了淀粉样蛋白的形成机制及其潜在的治疗策略。淀粉样蛋白是一类在人体内极易发生错误折叠并形成不可溶性纤维的蛋白质。当这些蛋白质在组织中堆积时，会对器官功能造成严重损害，进而引发疾病。迄今为止，研究人员已确认了36种易于形成淀粉样纤维的“淀粉样变”蛋白（amyloidogenic proteins）。这些蛋白质虽然在结构和功能上各有差异，但它们均具备共同的特点，即具有独特的β-折叠结构（β-sheet structure）。在正常生理条件下，这些蛋白质存在于正确折叠和错误折叠之间的一种动态平衡状态。当由于衰老或遗传变异等原因导致这种平衡向错误折叠倾斜时，细胞的质量控制机制——未折叠蛋白反应（unfolded protein response）通常会抑制淀粉样蛋白的形成。然而，一旦这一机制失效，淀粉样纤维便可能在心脏、肝脏、肾脏、神经和肌肉等多个器官中沉积，从而严重影响器官的正常功能。例如，心脏的甲状腺素运载蛋白型淀粉样变（transthyretin amyloidosis，ATTR）是一种重要但常常未被诊断的心力衰竭原因。此前，这种疾病被认为较为罕见，但根据一项芬兰研究，在85岁以上的患者中，有约25%的患者在心脏中发现淀粉样蛋白沉积。淀粉样蛋白不仅在心脏中堆积，还可影响到肝脏、肾脏、神经系统及其他重要器官。在这些组织中，淀粉样蛋白的沉积会逐渐破坏器官的正常功能，进而导致严重的病理生理后果。例如，在阿尔茨海默病中，淀粉样β蛋白（amyloid-β）沉积在大脑中，形成典型的斑块，阻碍神经细胞之间的信号传导，进而影响认知功能。此外，淀粉样蛋白还会诱发局部炎症反应，进一步加剧对神经元的损害。淀粉样蛋白堆积的治疗现状目前，已有15种不同类型的系统性淀粉样变被确认，这些类型的淀粉样变由不同的前体蛋白引起，导致淀粉样纤维在组织中的形成和沉积。随着质谱技术的进步，研究人员得以更加精确地鉴别不同类型的淀粉样变，尤其是通过基于质谱的“霰弹枪”蛋白组学（shotgun proteomics）分析技术对淀粉样蛋白进行分型。在系统性淀粉样变的药物开发方面，甲状腺素运载蛋白（transthyretin，TTR）的治疗取得了最早的成功。TTR由肝脏分泌至血浆，其主要功能是运载甲状腺激素甲状腺素（thyroxine）和视黄醇（维生素A）。TTR相关的淀粉样变（ATTR）可能由散发性或遗传性错误折叠引起，药物开发者正在通过以下几种方式来控制这种错误折叠：抑制TTR的合成：例如，Alnylam Pharmaceuticals公司开发的siRNA药物Onpattro（patisiran）和Amvuttra（vutrisiran）通过干扰RNA的方式降低TTR的合成水平，主要用于治疗伴有多发性神经病（polyneuropathy）的ATTR患者。这些siRNA药物通过靶向TTR的mRNA，阻止其在肝脏中合成，从而有效减少血浆中TTR的水平，进而减轻淀粉样纤维的沉积。这些药物在临床试验中表现出了显著的疗效，降低了患者的神经损伤进展率。稳定TTR的四聚体结构：Pfizer公司的Vyndaqel（tafamidis）通过选择性结合并稳定TTR的功能性四聚体，防止其解离为易于聚集的单体。Acoramidis则是另一种TTR稳定剂，由BridgeBio的子公司Eidos Therapeutics开发，其在III期临床试验中表现出对心血管疾病显著的疗效。在III期试验中，Acoramidis在生存率、心血管相关住院率和六分钟步行测试中均优于安慰剂组，治疗组的30个月生存率为80.7%，而对照组为74.3%。TTR的稳定剂通过防止TTR四聚体的解离，从根本上减少了错误折叠的发生，从而阻止淀粉样纤维的形成，这对于减轻器官损伤尤为重要。破坏TTR淀粉样纤维：一些抗体疗法也在开发中，旨在直接清除淀粉样纤维。例如，Prothena Biosciences公司开发的Birtamimab能够选择性结合错误折叠的免疫球蛋白轻链，诱导淀粉样纤维的清除。在一项III期临床试验的后续分析中，使用Birtamimab联合标准治疗的患者在九个月的生存率为74%，而使用安慰剂联合标准治疗的患者生存率仅为49%。这种直接针对淀粉样纤维的治疗方式为患者提供了全新的治疗选择，尤其是在疾病晚期阶段。此外，其他几种抗体疗法也正在开发中。例如，AstraZeneca和Neurimmune联合开发的ALXN2220是一种针对错误折叠的TTR的单克隆抗体，其在I期临床试验中未表现出剂量限制性毒性，这为其后续的开发奠定了基础。针对淀粉样纤维的抗体疗法通过识别和结合错误折叠的蛋白质，启动体内的免疫系统进行清除，从而减少淀粉样纤维对组织的损伤。淀粉样变治疗的新希望一个备受关注的发现是，有些类型的淀粉样变可以自发逆转。例如，由伦敦大学学院（UCL）的Julian Gillmore领导的一项研究发现，在1663名心肌病型甲状腺素运载蛋白淀粉样变（ATTR-CM）患者中，有三名患者通过抗体免疫反应成功逆转了淀粉样蛋白的沉积，心脏功能恢复至接近正常水平。虽然这种自发逆转的情况极为罕见，但这一发现为抗体疗法的开发提供了新的研究方向。目前，研究人员正在开发针对淀粉样纤维的单克隆抗体，例如英国公司Immutrin的抗体研究。这些抗体被寄予厚望，能够清除淀粉样沉积物，并在现有治疗药物的基础上提供额外的临床收益。Immutrin公司的研究主要集中于如何有效地复制这些罕见的自发逆转情况，通过优化抗体的结构和功能，力求最大限度地激发患者体内的免疫系统以清除淀粉样蛋白。另一个有趣的发展是基因编辑技术在淀粉样变治疗中的应用。Intellia Therapeutics与再生元公司（Regeneron Pharmaceuticals）联合开发的基因编辑药物Nexiguran Ziclumeran（“nex-z”），利用CRISPR-Cas9技术靶向肝细胞中的TTR基因，以实现对TTR的长效沉默。相关的I期试验结果显示，这种基因编辑疗法能够在治疗28天内将TTR水平降低90%以上，并且在非人灵长类动物中，这种效果可持续至少两年。基因编辑技术通过直接对基因组进行修改，能够实现长效的治疗效果。Nexiguran Ziclumeran通过在肝细胞中永久敲除TTR基因，从而彻底阻止TTR蛋白的合成。这种“一次治疗，长期有效”的方法在临床上具有巨大潜力，尤其是对于那些无法通过传统治疗手段获益的患者。此外，Intellia还进行了I期剂量递增研究，测试了nex-z的再给药情况。三名最初接受低剂量治疗的参与者在接受第二次更高剂量的治疗后，安全性良好，未观察到严重的不良反应。淀粉样蛋白治疗的挑战与未来尽管抗淀粉样变药物取得了一定进展，但要实现对系统性淀粉样变的功能性治愈，仍面临诸多挑战。首先，不同类型的淀粉样变由不同的前体蛋白引起，其临床表现差异显著，这增加了疾病诊断和治疗的难度。此外，许多淀粉样变疾病的症状在早期较为隐匿，容易被忽略，导致很多患者在疾病的晚期才被确诊，这时候的治疗效果往往不理想。诊断的复杂性也是一个重大挑战。目前，淀粉样变的诊断主要依赖于组织活检和基于质谱的蛋白质组学分析，这些方法虽然在准确性上有保障，但操作复杂且具有侵入性。Attralus公司开发了一种基于p5R多肽的泛淀粉样成像剂AT-01，这种成像剂能够结合所有类型的淀粉样纤维，并用于正电子发射断层扫描（PET）成像，从而提供了一种非侵入性的诊断方法。在治疗方面，研究人员还在尝试开发能够针对多种淀粉样纤维的“泛淀粉样”治疗药物。例如，Attralus公司开发的AT-02是一种由结合泛淀粉样纤维的肽段和人源化IgG1单克隆抗体融合而成的药物，旨在触发免疫反应以清除淀粉样沉积。该方法的独特之处在于，它并不依赖于特定类型的错误折叠蛋白，而是通过识别所有淀粉样纤维的共同结构特征来实现治疗。通过这种方法，可以有效地减少对特定前体蛋白的依赖，从而提高治疗的广谱性。淀粉样蛋白的沉积不仅与特定疾病相关，还与广泛的蛋白质错误折叠病症密切相关。例如，在肌萎缩侧索硬化症（ALS）中，超氧化物歧化酶1（superoxide dismutase 1，SOD1）和TAR DNA结合蛋白（TDP-43）之间的相互作用被认为是疾病的病理机制之一。这些蛋白质的错误折叠和聚集会损害神经元的正常功能，导致运动神经元的退化和死亡，最终引发ALS的进行性肌肉无力和萎缩。在一项针对SOD1和TDP-43相互作用的研究中，研究人员发现，这种相互作用可能是一种瞬时的“朊病毒样”播散机制，可能是ALS发病的原因之一。此外，研究显示，一种名为Telbivudine的核苷类似物能够在小鼠模型中缓解由SOD1聚集引起的神经毒性，为ALS患者提供了新的治疗方向。这些发现为开发针对ALS的新疗法提供了重要的理论基础，并为未来的临床试验指明了方向。淀粉样蛋白研究领域正在经历一个快速发展的时期，新技术的应用和新药物的开发使得这一领域的治疗前景日益明朗。未来的研究将集中于如何提高诊断的准确性和便利性、进一步优化现有治疗策略以及开发出能够全面覆盖多种类型淀粉样变的泛治疗方案。参考文献 Sheridan, C. Amyloid is everywhere, but new treatments could stop the toxic build up. Nat Biotechnol 42, 1625–1628 (2024). https://doi.org/10.1038/s41587-024-02471-1 责编|探索君排版|探索君转载请注明来源于【生物探索】声明：本文仅用于分享，不代表平台立场，如涉及版权等问题，请尽快联系我们，我们第一时间更正，谢谢！ End 往期精选围观一文读透细胞死亡(Cell Death) | 24年Cell重磅综述（长文收藏版）热文 Cell | 是什么决定了细胞的大小？热文 Cell | AI取代科研人员还有多远？热文新英格兰 | 司美格鲁肽（semaglutide）又有新发现：助力关节炎治疗热文 CRISPR技术进化史 | 24年Cell 综述

2024-10-23

·neurimmune.com

Neurimmune Announces Publication in Clinical Pharmacology & Therapeutics of The Prediction of Cardiac ATTR Depletion by ALXN2220

Neurimmune today announced that the translational PK/PD model relating to the human antibody ALXN2220 (formerly NI006) have been published in the current issue of Clinical Pharmacology & Therapeutics. The manuscript “Prediction of cardiac ATTR depletion by NI006 (ALXN2220) using mechanistic PK/PD modeling” describes the mechanistic pharmacokinetic and pharmacodynamic model used to predict drug exposure and its effects on cardiac transthyretin amyloid load.1 ALXN2220 is an investigational human monoclonal antibody designed to deplete amyloid deposits in transthyretin amyloidosis with cardiomyopathy (ATTR-CM).2,3 The mechanistic PK/PD model described by Michalon et al. provided important predictions to select a safe and potentially efficacious dose range and treatment duration for a proof-of-concept clinical Phase 1b study of ALXN2220. The model enabled the integration of preclinical results into the clinical trial design and provided predictions that were in good agreement with the observed primary results of the Phase 1b study recently published in The New England Journal of Medicine. “We are excited about the predictive accuracy of our model which supported the translation of our preclinical findings on ALXN2220-mediated TTR amyloid depletion into the design of a successful Phase 1b clinical trial of ALXN2220,” said Jan Grimm, PhD, Chief Scientific Officer of Neurimmune. “We would like to thank Alexion and Lyo-X for the close collaboration and look forward to Alexion’s continued clinical development of this novel treatment with the potential to transform the course of ATTR amyloidosis.” ATTR-CM is a systemic, progressive and life-threatening disease caused by the deposition of misfolded transthyretin (TTR), which can lead to heart failure. Despite advances in slowing disease progression, there is no available treatment option designed to deplete TTR from the heart to revert cardiac dysfunction. In 2022, Neurimmune entered into an exclusive global collaboration and license agreement with Alexion, AstraZeneca Rare Disease for ALXN2220. Neurimmune is responsible for the completion of the Phase 1b clinical study on behalf of Alexion. Aside from the Phase 1b trial, Alexion is responsible for further clinical development, manufacturing, and commercialization of ALXN2220. Alexion, AstraZeneca Rare Disease, is currently conducting the Phase 3 DepleTTR-CM clinical study to assess the efficacy and safety of ALXN2220 as an add-on treatment to the standard of care for patients with ATTR-CM. 1 Michalon et al., Clin Pharm Ther 2024; in press, doi:10.1002/cpt.3455 2 Garcia-Pavia et al., N Engl J Med 2023 3 Michalon et al., Nat Commun 2021; 12(1):3142 Neurimmune is a biopharmaceutical company translating human immune memory into antibody therapeutics. Neurimmune develops drug candidates for CNS and related protein aggregation diseases including Alzheimer’s disease, amyotrophic lateral sclerosis, frontotemporal dementia and ATTR cardiomyopathy. With its Reverse Translational MedicineTM technology, Neurimmune discovered the brain amyloid depleter NI101SQ for Alzheimer’s disease, anti-SOD1 antibody AP-101 for ALS and the anti-ATTR antibody ALXN2220 (formerly NI006) for ATTR cardiomyopathy, programs being currently evaluated in clinical trials. John Capodanno (US) john.capodanno@dentonsglobaladvisors.com Martin Meier-Pfister (Switzerland) media@neurimmune.com

临床1期引进/卖出临床3期临床2期

2024-10-14

·neurimmune.com

FDA Fast Track Designation for ALXN2220 for Depletion of Cardiac ATTR

Neurimmune today announced that the U.S. Food and Drug Administration (FDA) has granted Alexion, AstraZeneca Rare Disease Fast Track designation for the development of ALXN2220 (formerly NI006) for the treatment of transthyretin amyloidosis with cardiomyopathy (ATTR-CM). ATTR-CM is a systemic, progressive and life-threatening disease caused by the deposition of misfolded transthyretin (TTR), which can lead to heart failure. Despite advances in slowing disease progression, there is no available treatment option designed to deplete TTR from the heart to revert cardiac dysfunction. The Fast Track designation was granted based on the results of a Phase 1b trial conducted by Neurimmune and published in The New England Journal of Medicine in 2023.1 "In our Phase 1b trial intravenously administered ALXN2220 reduced cardiac tracer uptake and extracellular volume. The reduction of these surrogate markers of cardiac amyloid load suggests that ALXN2220 can induce the depletion of cardiac amyloid deposits by the immune system. This is a novel therapeutic mechanism with potential to restore cardiac function in patients suffering from ATTR amyloidosis,” said Christoph Hock, MD, Chief Medical Officer of Neurimmune. “We look forward to Alexion’s continued development of ALXN2220 and are very pleased the FDA’s Fast Track designation will help accelerate this effort.” ALXN2220 is an investigational human monoclonal antibody currently being evaluated in the Phase 3 DepleTTR-CM trial to assess its efficacy as an add-on treatment to the standard of care for patients with ATTR-CM. The primary endpoint is a composite of all-cause mortality and cumulative frequence of cardiovascular clinical events. The Fast Track designation is granted to expedite the review of drugs to treat serious conditions and address an unmet medical need. The designation allows for more frequent interactions with the FDA, and potentially in the future, Accelerated Approval and Priority Review in the U.S. In 2022, Neurimmune entered into an exclusive global collaboration and license agreement with Alexion, AstraZeneca Rare Disease for ALXN2220. Neurimmune is responsible for the completion of the Phase 1b clinical study on behalf of Alexion, with Alexion incurring certain trial costs. Aside from the Phase 1b trial, Alexion is responsible for further clinical development, manufacturing, and commercialization of ALXN2220. 1Garcia-Pavia et al., N Engl J Med 2023 Neurimmune is a biopharmaceutical company translating human immune memory into antibody therapeutics. Neurimmune develops drug candidates for CNS and related protein aggregation diseases including Alzheimer’s disease, amyotrophic lateral sclerosis, frontotemporal dementia and ATTR cardiomyopathy. With its Reverse Translational MedicineTM technology, Neurimmune discovered the brain amyloid depleter NI101SQ for Alzheimer’s disease, anti-SOD1 antibody AP-101 for ALS and the anti-ATTR antibody ALXN2220 (formerly NI006) for ATTR cardiomyopathy, programs being currently evaluated in clinical trials. John Capodanno (US) john.capodanno@dentonsglobaladvisors.com Martin Meier-Pfister (Switzerland) media@neurimmune.com

临床1期引进/卖出快速通道

100 项与 NI-006 相关的药物交易

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适应症	最高研发状态	国家/地区	公司	日期
转甲状腺素运载蛋白淀粉样变性	临床3期	捷克	阿斯利康全球研发（中国）有限公司	2024-01-11
转甲状腺素运载蛋白淀粉样变性	临床3期	美国	阿斯利康全球研发（中国）有限公司	2024-01-11
转甲状腺素运载蛋白淀粉样变性	临床3期	德国	阿斯利康全球研发（中国）有限公司	2024-01-11
转甲状腺素运载蛋白淀粉样变性	临床3期	希腊	阿斯利康全球研发（中国）有限公司	2024-01-11
转甲状腺素运载蛋白淀粉样变性	临床3期	澳大利亚	阿斯利康全球研发（中国）有限公司	2024-01-11
转甲状腺素运载蛋白淀粉样变性	临床3期	意大利	阿斯利康全球研发（中国）有限公司	2024-01-11
转甲状腺素运载蛋白淀粉样变性	临床3期	波兰	阿斯利康全球研发（中国）有限公司	2024-01-11
转甲状腺素运载蛋白淀粉样变性	临床3期	荷兰	阿斯利康全球研发（中国）有限公司	2024-01-11
转甲状腺素运载蛋白淀粉样变性	临床3期	瑞士	阿斯利康全球研发（中国）有限公司	2024-01-11
转甲状腺素运载蛋白淀粉样变性	临床3期	挪威	阿斯利康全球研发（中国）有限公司	2024-01-11

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT04360434 (NI006-101, Literature) 人工标引	临床1期	甲状腺素运载蛋白淀粉样变心肌病	40	NI006	(憲鑰積願廠繭獵窪醖餘) = The use of NI006 was associated with no apparent drug-related serious adverse events. 願齋製願願網廠鑰鏇構 (餘網顧夢構膚網簾壓壓 )	积极	2023-07-30
				placebo